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  • Author or Editor: Xinhua Wang x
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The Stonyhard peach fruit mutation has been used to study softening and textural changes during ripening. Without ethylene exposure, firmness of Stonyhard remains fairly constant at room temperature. When exposed to 1 or 100 ppm C2H2 for 48 hours, fruits soften at a rate consistent with control fruit (`Cresthaven') to a similar firmness. However, 1 ppm—treated fruit attains a normal juicy texture, while 100 ppm—treated fruit attains a pasty texture. Control fruit softened to a normal juicy texture with either ethylene treatment. Cell wall endopolygalacturonase (endo-PG) was not detectable in Stonyhard fruit without C2H2 exposure; it increased at a rate similar to control fruit when exposed to 1 ppm C2H2, and was double that of 1 ppm for fruit exposed to 100 ppm for up to 48 hours. Low levels of endo-PG were detected in control fruit not exposed to C2H2; 1 ppm treatment led to a normal increase, which was comparable to that in Stonyhard. However, endo-PG in 100 ppm—treated fruit was very similar to that of 1 ppm for up to 24 hours, though high levels of endo-PG were observed at 48 hours. Attainment of the pasty texture in 100 ppm—treated Stonyhard fruit may have been related to release of large quantities of pectic polysaccharides as a result of the sudden increase in endo-PG activity. Work was supported by USDA grant 96-34150-2540 and the Oklahoma Agricultural Experiment Station.

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The physiological role of arginase in nitrogen remobilization processes from protein degradation during seed germination has well been described in several species. However, very little is known about its possible roles in plant stress responses. Treatment of tomato fruit (Solanum lycopersicum L.) with 0.05 mm methyl jasmonate (MeJA) enhanced transcription levels of arginase genes, especially LeARG2. Chilling injury (CI) of fruit treated with 0.05 mm MeJA for 12 hours was also effectively alleviated, as manifested by decreases in CI index, electrolyte leakage, and malondialdehyde (MDA) content. To investigate the potential role of arginase in MeJA-induced chilling tolerance, fruit were treated with MeJA or the arginase inhibitor Nω-hydroxy-nor-l-arginine (nor-NOHA) combined with MeJA and then stored at 2 °C for 28 days. MeJA-induced arginase activity was strongly inhibited and the reduction of CI by MeJA was nearly abolished by the inhibitor. In addition, MeJA treatment increased the activities of superoxide dismutase (SOD), catalase (CAT), and ascorbate peroxidase (APX); inhibited peroxidase (POD) activities; and promoted proline and polyamines accumulation. These effects were partially counteracted by nor-NOHA; putrescine accumulation, however, was unaffected by the inhibitor. Our results indicate that arginase may be involved in MeJA-induced chilling tolerance, possibly by ameliorating the antioxidant enzyme system of fruit and increasing proline levels.

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